CASE

Asthma in Pregnancy

Counselor :
Dr. H. Achmad Djaenudin, SpOG

by :

Agustinus E. Wijaya
11-2007-053

Obstetric And Gynecology Department

Period February 4th 2007 April 12nd 2008
Medical Faculty UKRIDA
Bhakti Yudha Hospital
Depok

KRIDA WACANA CHRISTIAN of UNIVERSITY

Medical Faculty
Obstretric and gynecologic Case
Student Name
NIM
Counselor

: Agustinus E. Wijaya
: 11-2007-053
: Dr.H.Achmad Djaenudin, SpOG

Pasient Identity
Name
Age
Religion
Gender
Last education
Occupation
Tribe
Date of admission

: Mrs. An
: 26 years old
: Moslem
: Woman
: Senior high school
: Housewife
: Javanese
: March 9th, 2008

Husband name
Age
Religion
Last education
Occupation
Address
Status

: Mr. S
: 30 years old
: Moslem
: Senior high school
: Employee
: Jl. Citayam II no. 4 RT 03/RW 04 Pancoran Mas, Depok
: Marriage

A. ANAMNESIS
Take from
Date

: autoanamnesis and Medical Record

: March 9th, 2008
Time : 04.20 pm

Primary Subjective:
Breathlessness becoming heavier since 1 day before entering hospital.
Addition subjective : cough.
History of Present Pregnancy :
3 last months she has ever been opname in Bhakti Yudha hospital because
asthma and experiences treatment during 2 days. She confessed gets inhalant for
asthma just in case she has a breathlessness attack.
During more than 2 months she told that she had been getting mild attack of
asthma but she can control the asthma with her inhalant drug.

1 day before before entered hospital but at night, she had asthma attack. This
time, the asthma attack became worse than before so the inhaler can not work in dose.
But after she use that drug she felt better even her breathing was not as normal as
usual.
Evening before entered hospital, she came to Bhakti Yudha Hospital with
asthma attack became more worse than before. She didnt know why she got this
attack. She just told ask that she was alergic to sea food.
She is being in period of pregnancy. Last menstruation date is october 15 th,
2007
Past Obstetrical history :
Non
Obstetrical History

: G1 P0 A0 gestational age 21 weeks

Menstrual history
:
Menarche
Menstrual duration
cycle
regular cycle
First day of the last Mentruation
Partum estimation

: 13 years old
: 7 days
: regular
: 30 days
: October 15th, 2007
: July 22th, 2008

History of past illness :

- Smoking history denied
- Hypertension denied
- endocrine denied
- Heart disease denied
- Tuberculosis denied
- Kidney disease denied
- Drug allergy denied
- Astma
- Seafood allergy
B. Phisycal Examination
1. General status
General impression
Consciousness
Blood pressure
Pulse
Temperature
Respiratory rate
Body height
Body weight
Head
Eyes
Hearts

: well
: compos mentis
: 130/90 mmHg
: 120 x/ minute
: 36,2 0C
: 40 x/ minute
: 164 cm
: 65 kg
: Normocephaly , black hair, normal distribution
: anemic conjunctiva -/- icteric sclera -/: regular S1-S2, no murmur nor gallop

Pulmo
,wheezing(+)
Extremities

2. Obstetric status :
- Abdomen :
Inspection
Palpation

: bilateral vesicular breath sound, no rales

: edeme +

: seen the stomach enlarged, linear nigra and stretch mark (-)
: Fundus height 25 cm.

Fetal weight estimation by Johnson-Tausak :

= (25 -12) x 155
= 2015 kg
Doppler auscultation : fetal heart rate 134 beats per minute
His : -Anogenital :
- vulva / urethae
: not done
- inspeculum examination
: not done
- vagina wall
:
- Fluor / Fluxus
:
- Portio
:
- serviks dilatation
:
- amnionic
:
- colour of amnion fluid :
- lacmus test
:
- Vaginal Touche
: not done
- Portio
:
- serviks dilatation
:
- amnionic
:
- Head Hodge I
C. Supportive examination
Laboratory March 9th, 2008
Hb
: 13,1 g/dL
Leucocyte
: 15.000
/uL
Ht
: 39 %
Trombocyte : 258.000
/uL
USG : One live intra uterine
Placenta infront
Amniotic fluid enough
Pregnancy age 24 weeks
D. DIAGNOSIS
Maternal
: Gravidity 1, Parity 0, pregnancy age 21 weeks with asthma
Fetal
: One live intra uterine fetal

E. MANAGEMENT
Planning of diagnose :
CTG
Planning of theraphy :
Nebulizer ventolin III
Aminofilin 1 vial in 500 cc KA-EN 3B 20 drops/minute.
Amoxsan 500 mg 3x1
Dextamin 2x1
Planning of education :
Avoid to contact with the allergen, like food or the other that made the
patient allegy.
Explain to patient and the family about condition of patient and about
the risk will be happen for the maternal and fetal.
VI. PROGNOSIS
Maternal
Fetal

: dubia
: dubia

Follow up
08/03/2008
S : breathlessness
O: General status
General impression
Consciousness
Blood pressure
Pulse
Temperature
Respiratory rate

: well
: compos mentis
: 8110/70mmHg
: 8 x/ minute
: 35,3 0C
: 28 x/ minute, rales +, wheezing +

Obstetric status :
Fundus height : 25 cm
Fetal heart rate : 154 bpm
A: Gravidity 1, Parity 0, pregnancy age 21 weeks with asthma
P : - Bedrest
- avoid allergen
Th : O2 3liters/minute
Nebulizer ventolin III
Aminofilin 1 vial in 500 cc KA-EN 3B 8hours/kolf.

09/03/2008
S : influenza
O: General status
Consciousness
Blood pressure
Pulse
Temperature
Respiratory rate

: compos mentis
: 90/60 mmHg
: 90 x/ minute
: 36 0C
: 32 x/ minute, rales +, wheezing +

Obstetric status :
Fundus height : 25 cm
Fetal heart rate : 143 bpm
A: Gravidity 1, Parity 0, pregnancy age 21 weeks with asthma not recover
P : - Bedrest
- avoid allergen
Th : O2 3liters/minute
Nebulizer ventolin III if the patient breathlessness
Medixon injection in need.
Aminofilin 1 vial in 500 cc KA-EN 3B 10hours/kolf.

10/03/2008
S : none sigh
O: General status
General impression
: well
Consciousness
: compos mentis
Blood pressure
: 100/60 mmHg
Pulse
: 80 x/ minute
Temperature
: 36,7 0C
Respiratory rate
: 16 x/ minute,wheezing +
Obstetric status :
Fundus height : 25 cm
Fetal heart rate : 145 bpm
A: Gravidity 1, Parity 0, pregnancy age 21 weeks with asthma recover
P : - Bedrest
- avoid allergen
Th :
Nebulizer ventolin III if the patient breathlessness
Dextamin 2 x 1
Aminofilin 1 vial in 500 cc KA-EN 3B 10hours/kolf.
Amoxicillin 3 x 500 mg

ASTHMA
According to the Centers for Disease Control and Prevention (2004a), about 7 percent
of the general population currently has asthma. In a national survey, Kwon and
associates (2003) estimated current asthma prevalence in pregnant women to be 5 to 9
percent. Moreover, Namazy and Schatz (2005) reported that the prevalence of asthma
in pregnant women appears to be increasing. Status asthmaticus, the most severe form
of asthma, complicates about 0.2 percent of pregnancies (Mabie and associates,
1992).
Pathophysiology
Asthma is a chronic inflammatory airway disorder with a major hereditary
component. Increased airway responsiveness and inflammation have been linked to
candidate genes on chromosomes 5, 6, 11, 12, 14, and 16 (Tattersfield and colleagues,
2002), including the high-affinity IgE receptor, the cytokine gene cluster, and the Tcell antigen receptor. These conditions have also recently been linked to mutations of
the ADAM-33 gene on the short arm of chromosome 20 (Shapiro and Owen, 2002).
There inevitably is an environmental allergic stimulant in susceptible individuals, for
example, influenza or cigarette smoke (Hartert and colleagues, 2003; Sheffield, 2005).
The hallmarks of asthma are reversible airway obstruction from bronchial smooth
muscle contraction, mucus hypersecretion, and mucosal edema. There is airway
inflammation and responsiveness to a number of stimuli, including irritants, viral
infections, aspirin, cold air, and exercise. Mast cell activation by cytokines mediates
bronchoconstriction by release of histamines, prostaglandin D 2, and leukotrienes.
Because F-series prostaglandins and ergonovine exacerbate asthma, these
commonly used obstetrical drugs should be avoided if possible.
Clinical Course
Asthma represents a broad spectrum of clinical illness ranging from mild wheezing to
severe bronchoconstriction. The functional result of acute bronchospasm is airway
obstruction and decreased airflow. The work of breathing progressively increases, and
patients present with chest tightness, wheezing, or breathlessness. Subsequent
alterations in oxygenation primarily reflect ventilationperfusion mismatching,
because the distribution of airway narrowing is uneven.
The clinical stages of asthma are summarized in Table 463. With mild disease,
hypoxia initially is well compensated by hyperventilation, as reflected by a normal
arterial PO2, decreased PCO2, and resultant respiratory alkalosis. As airway narrowing
worsens, ventilationperfusion defects increase, and arterial hypoxemia ensues. With
severe obstruction, ventilation becomes impaired because fatigue causes early CO2
retention. Because of hyperventilation, this may only be seen initially as an arterial
PCO2 returning to the normal range. Finally, with critical obstruction, respiratory
failure follows, characterized by hypercapnia and acidemia.

Table 463. Clinical Stages of Asthma

Stage

PO2

PCO2

pH

FEV1 (% predicted)

Mild respiratory alkalosis Normal

6580

Respiratory alkalosis

5064

Danger zone
Respiratory acidosis

Normal Normal 3549

<35

Modified after Barth and Hankins (1991), with permission.

Although these changes are generally reversible and well tolerated in the healthy
nonpregnant individual, even early stages of asthma may be dangerous for the
pregnant woman and her fetus. The smaller functional residual capacity and the
increased effective shunt render her more susceptible to hypoxia and hypoxemia.
Effects of Pregnancy on Asthma
There is no evidence that pregnancy has a predictable effect on underlying asthma. In
two prospective studies of more than 500 pregnant women, about equal thirds of the
group either improved, remained unchanged, or clearly worsened (Schatz and
colleagues, 1988; Stenius-Aarniala and associates, 1988). Baseline asthma severity
correlates with asthma morbidity during pregnancy (Schatz and associates, 2003).
With mild disease, 13 percent of women had an exacerbation; with moderate disease,
26 percent did; and with severe asthma, about 50 percent did. In the same study, about
20 percent of women with mild or moderate asthma had an intrapartum exacerbation.
Conversely, Wendel and associates (1996) observed this in only 1 percent of women.
Mabie and co-workers (1992) reported an 18-fold increased risk of exacerbation
following cesarean versus vaginal delivery.
Pregnancy Outcome
Generally, unless there is severe disease, asthma has relatively minor effects on
pregnancy outcome. Table 464 shows maternal and perinatal outcomes in more than
9000 pregnancies complicated by asthma. Most studies describe a slightly increased
incidence of preeclampsia, preterm labor, low-birthweight infants, and perinatal
mortality. In the observational study by the MaternalFetal Medicine Units Network,
delivery before 37 weeks was not increased among the 1687 pregnancies complicated
by asthma compared with that of 881 controls (Dombrowski and colleagues, 2004a).
However, for the 52 women with severe asthma, the rate was increased about twofold.
Similarly, Bracken and colleagues (2003) found that preterm delivery was only
minimally increased in women with asthma and fetal growth restriction increased
with asthma severity. In a prospective evaluation of 656 asthmatic pregnant women

and 1052 nonasthmatic pregnant controls, Triche and co-workers (2004) found that
women with moderate to severe asthma, regardless of treatment, are at increased risk
of preeclampsia.
Table 464. Maternal and Perinatal Outcomes in Pregnancies Complicated by Asthma

Perinatal Outcomes (Percent)

Study

Number (n = Pregnancy
9291)
Hypertension

Growth
Restriction

Alexander et al
(1998)

817

Demissie et al
(1998)

2289

15

18

Liu et al (2001)

2193

13

12

10

Bracken et al
(2003)

872

NS

8.5

8.5

Ramsey et al
(2003)

1381

NS

1.7

15

Dombrowski et al 1739
(2004)

12.2a

Approximate
average

11

Preterm
Delivery

Not
12

Not

16a

12

NS = not stated.
a

Incidence not significantly different compared with controls.

Life-threatening complications from status asthmaticus include muscle fatigue with

respiratory arrest, pneumothorax, pneumomediastinum, acute cor pulmonale, and
cardiac arrhythmias. Maternal and perinatal mortality is substantively increased when
mechanical ventilation is required.
Fetal Effects
In the Network study cited above, asthma was not associated with significant adverse
neonatal sequelae (Dombrowski and co-workers, 2004a). Severe asthma was
uncommon, and when respiratory alkalosis developed, both animal and human studies
have suggested that fetal hypoxemia may occur well before maternal oxygenation is
compromised (Rolston and associates, 1974). Fetal compromise is hypothesized to
result from decreased uterine blood flow, decreased maternal venous return, and an
alkaline-induced leftward shift of the oxyhemoglobin dissociation curve. With
maternal hypoxemia, the fetus responds with decreased umbilical blood flow,
increased systemic and pulmonary vascular resistance, and decreased cardiac output.

Recent observations by Bracken and colleagues (2003) confirm that the incidence of
fetal growth restriction increases with severity of asthma. The realization that the fetus
may be seriously compromised as asthma severity increases underscores the need for
aggressive management of all pregnant women with acute asthma. Monitoring the
fetal response is, in effect, an indicator of maternal status.
In addition, possible teratogenic or adverse fetal effects of drugs given to control
asthma are a concern. As discussed in Chapter 14 (Asthma Medications), considerable
published data indicates there is no evidence that commonly used anti-asthmatic drugs
are harmful (Nelson-Piercy, 2001; Schatz, 2001; Wendel, 2001).
Clinical Evaluation
The subjective severity of asthma frequently does not correlate with objective
measures of airway function or ventilation. Clinical examination also is inaccurate as
a predictor of severity. Useful clinical signs include labored breathing, tachycardia,
pulsus paradoxus, prolonged expiration, and use of accessory muscles. Signs of a
potentially fatal attack include central cyanosis and altered consciousness.
Arterial blood gas analysis provides objective assessment of maternal oxygenation,
ventilation, and acidbase status. With this information, the severity of an acute attack
can be assessed (see Table 463). In a prospective evaluation, however, Wendel and
associates (1996) found that routine blood gas analysis did not help direct care in
most pregnant women. Importantly, the results must be interpreted in relation to
normal values for pregnancy. For example, a PCO2 greater than 35 mm Hg with a pH
less than 7.35 is consistent with hyperventilation and CO 2 retention in a pregnant
woman.
Pulmonary function testing is now routine in the management of chronic and acute
asthma. Sequential measurement of the FEV1 is the single best measure reflecting
severity. An FEV1 less than 1 L, or less than 20 percent of predicted, correlates with
severe disease, defined as hypoxia, poor response to therapy, and a high relapse rate
(Noble and colleagues, 1988). The peak expiratory flow rate (PEFR) correlates well
with the FEV1, and it can be measured reliably with inexpensive portable meters.
Brancazio and associates (1997) showed that the PEFR did not change over the course
of pregnancy in normal women.
Management of Chronic Asthma
According to the National Asthma Education Program (1997), effective management
of asthma during pregnancy includes:
1. Objective assessment of pulmonary function and fetal well-being.
2. Avoidance or control of environmental precipitating factors.
3. Pharmacological therapy.
4. Patient education.

In general, women with moderate to severe asthma are instructed to measure and
record their PEFR twice daily. Predicted values range from 380 to 550 L/min. Each
woman has her own baseline value, and therapeutic adjustments can be made using
this.
Treatment depends on the severity of disease. Drugs recommended for home
management are listed in Table 465. For mild asthma, inhaled
-agonists as
needed are usually sufficient. Inhaled corticosteroids are the preferred treatment for
persistent asthma. Inhalations are administered every 3 to 4 hours as needed. The goal
is to reduce the use of
-agonists for symptomatic relief. A case-control study
from Canada with a cohort of over 15,600 nonpregnant women with asthma showed
that inhaled corticosteroids reduced hospitalizations by 80 percent (Blais and
associates, 1998). In pregnant women, Wendel and colleagues (1996) reported a 55percent reduction in readmissions for severe exacerbations in women given
maintenance inhaled corticosteroids along with

-agonist therapy.

Table 465. Step Therapy of Chronic Asthma During Pregnancy

Severity
Mild
intermittent
Mild persistent

Step Therapy
Inhaled
salmeterol

-agonistsisoetharine, metaproterenol, isoproterenol,

Inhaled

-agonistsas above

Inhaled cromolyncontinue if taking prior to pregnancy with good

response
Substitute inhaled corticosteroids if no responsebeclomethasone,
budesonide, triamcinolone
Moderate
persistent

Inhaled

-agonists as above

Inhaled corticosteroids as above, add oral theophylline and/or

inhaled salmeterol if inhaled medium-dose steroids inadequate
Severe
persistent

For moderate as above plus oral corticosteroidsburst for active

symptoms, alternate-day or daily if necessary

From National Asthma Education and Prevention Program Expert Panel Report 2
(1997) and American College of Obstetricians and Gynecologists, American College
of Allergy, Asthma, and Immunology (2000).
Cromolyn and nedocromil inhibit mast cell degranulation. They are ineffective for
acute asthma and are taken chronically for prevention. They likely are not superior to
inhaled corticosteroids.

Theophylline is a methylxanthine, and its various salts are bronchodilators and

possibly anti-inflammatory agents. These drugs have been used less frequently since
inhaled steroids became available. Some theophylline derivatives are considered
useful for oral maintenance therapy if the initial response is not optimal to inhaled
corticosteroids and
-agonists (see Table 465). Dombrowski and colleagues
(2004b) conducted a randomized trial with nearly 400 pregnant women with moderate
asthma. Oral theophylline was compared with inhaled beclomethasone for
maintenance. In both groups, about 20 percent had exacerbations. Women taking
theophylline had a significantly higher discontinuation rate because of side effects.
Pregnancy outcomes were similar in both the women who received theophylline and
those who received beclomethasone.
Leukotriene modifiers inhibit their synthesis and include zileuton, zafirinkast, and
montelukast. These drugs are given either orally or by inhalation for prevention, but
they are not effective for acute disease. For maintenance, they are used in conjunction
with inhaled steroids to allow minimal dosing. Ducharme (2002) reviewed all
randomized trials conducted through 2001 and concluded that these agents resulted in
only slightly improved asthma control. There is little experience with their use in
pregnancy.
Management of Acute Asthma
Treatment of acute asthma during pregnancy is similar to that for the nonpregnant
asthmatic. An exception is a significantly lowered threshold for hospitalization.
Intravenous hydration may help clear pulmonary secretions, and supplemental oxygen
is given by mask after a blood gas sample is obtained if indicated. The therapeutic aim
is to maintain the PO2 greater than 60 mm Hg, and preferably normal, along with 95percent oxygen saturation. Baseline pulmonary function testing includes FEV 1 or
PEFR. Continuous pulse oximetry and electronic fetal monitoring may provide useful
information.
First-line therapy for acute asthma includes a
-adrenergic agonist, either
terbutaline, albuterol, isoetharine, epinephrine, isoproterenol, or metaproterenol,
which is given subcutaneously, taken orally, or inhaled. These drugs bind to specific
cell-surface receptors and activate adenylyl cyclase to increase intracellular cyclic
AMP and modulate bronchial smooth muscle relaxation. The long-acting preparations
are used for outpatient therapy.
Corticosteroids should be given early to all patients with severe acute asthma
(National Heart, Lung and Blood Institute, 1993). Recommended doses, which are
probably higher than necessary, are intravenous methylprednisolone, 40 to 60 mg,
every 6 hours. Equipotent doses of hydrocortisone by infusion or prednisone orally
can be given instead. Because their onset of action is several hours, whether given
intravenously or by aerosol, steroids are given along with
-agonists for acute
asthma. In one audit, Cydulka and associates (1999) reported that pregnant women
presenting with asthma to academic medical center emergency departments were
given systemic corticosteroids in only 44 percent of cases.

Further management depends on the response to therapy. If initial therapy with

agonists is associated with improvement of FEV1 or PEFR to above 70 percent of
baseline, then discharge can be considered. Some women may benefit from 23-hour
observation. Alternatively, for the woman with obvious respiratory distress, or if the
FEV1 or PEFR is less than 70 percent of predicted after three doses of

-agonist,

admission is advisable. Intensive therapy includes inhaled

-agonists, intravenous
corticosteroids, and close observation for worsening respiratory distress or fatigue in
breathing (Wendel and colleagues, 1996).
Status Asthmaticus and Respiratory Failure
Severe asthma of any type not responding after 30 to 60 minutes of intensive therapy
is termed status asthmaticus. Braman and Kaemmerlen (1990) have shown that
management of nonpregnant patients with status asthmaticus in an intensive care
setting results in a good outcome in most cases. Consideration should be given to
early intubation when maternal respiratory status worsens despite aggressive
treatment (see Table 463). Fatigue, carbon dioxide retention, and hypoxemia are
indications for mechanical ventilation.
Labor and Delivery
Maintenance medications are continued through delivery. Stress-dose corticosteroids
are administered to any woman given systemic steroid therapy within the preceding 4
weeks. The usual drug is 100 mg of hydrocortisone given intravenously every 8
hours. The PEFR or FEV1 should be determined on admission and serial
measurements made if symptoms develop.
A nonhistamine-releasing narcotic, such as fentanyl, may be preferable to meperidine
for labor. Epidural analgesia for labor is ideal. For surgical delivery, conduction
analgesia is preferred because tracheal intubation can trigger severe bronchospasm.
Refractory postpartum hemorrhage is treated with prostaglandin E 2 or other
uterotonics instead of prostaglandin F2
, which may cause significant
bronchospasm in asthmatic patients. Oxygen desaturation following 15-methyl PGF 2
has been reported in women without reactive airway disease (Hankins and
colleagues, 1988)

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